P K Pang

University of Alberta, Edmonton, Alberta, Canada

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Publications (156)476.81 Total impact

  • American Journal of Hypertension 01/2002; 14(12):1273-5. · 3.40 Impact Factor
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    ABSTRACT: The activity of CVT-E002, an aqueous extract containing mainly oligosaccharides and polysaccharides from North American ginseng (Panax quinquefolium), as an immunobooster on murine spleen cells and peritoneal macrophages, was studied in-vitro. CVT-E002 stimulated the proliferation of normal mouse spleen cells, of which the major responding subpopulation was identified as B lymphocytes. CVT-E002 also activated peritoneal exudate macrophages leading to enhanced interleukin-1 (IL-1), interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-alpha) and nitric oxide (NO) production. In addition, CVT-E002 stimulated in-vivo immunoglobulin G (IgG) production in treated mice. These results identify some of the immunomodulating activities of CVT-E002 and suggest its use clinically for the modulation of immune responses.
    Journal of Pharmacy and Pharmacology 12/2001; 53(11):1515-23. · 2.16 Impact Factor
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    ABSTRACT: Alcoholic extracts of the roots and leaves of three Echinacea species (E. purpurea, E. angustifolia and E. pallida) were analysed for the presence of characteristic chemicals by HPLC directly coupled to ultraviolet absorbance and electrospray mass spectrometric detectors. The method permitted rapid characterization and tentative identification of a large number of caffeoyl conjugates and alkamides in all the samples investigated. The roots of the three species differed markedly in their contents of characteristic compounds. Cichoric acid and verbascoside predominated in extracts of E. purpurea root whereas cynarine and dodeca-2E,4E,8Z,10Z/E-tetraenoic acid isobutylamide were the major chemicals characteristic of E. angustifolia root extracts. Echinacoside and 6-O-caffeoylechinacoside predominated in extracts of E. pallida roots. Characteristic alkamides were also examined by electrospray tandem mass spectrometry (MS/MS) and these compounds provided characteristic fragmentation patterns. Extracts of the roots and leaves of all three species were found to have antioxidant properties in a free radical scavenging assay and in a lipid peroxidation assay.
    Journal of Pharmacy and Pharmacology 07/2001; 53(6):849-57. · 2.16 Impact Factor
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    ABSTRACT: A combination herbal product containing American ginseng extract, Panax quinquefolium, (200 mg) and Ginkgo biloba extract (50 mg) (AD-FX; CV Technologies, Edmonton, Alta.) was tested for its ability to improve the symptoms of attention-deficit hyperactivity disorder (ADHD). Open study. 36 children ranging in age from 3 to 17 years who fit the diagnostic criteria for ADHD. AD-FX capsules were taken twice a day on an empty stomach for 4 weeks. Patients were instructed not to change any other medications during the study. At the beginning of the study, after 2 weeks, and then at the end of the 4-week trial, parents completed the Conners' Parent Rating Scale--revised, long version, a questionnaire that assesses a broad range of problem behaviours (and was used as an indication of ADHD symptom severity). After 2 weeks of treatment, the proportion of the subjects exhibiting improvement (i.e., decrease in T-score of at least 5 points) ranged from 31% for the anxious-shy attribute to 67% for the psychosomatic attribute. After 4 weeks of treatment, the proportion of subjects exhibiting improvement ranged from 44% for the social problems attribute to 74% for the Conners' ADHD index and the DSM-IV hyperactive-impulsive attribute. Five (14%) of 36 subjects reported adverse events, only 2 of which were considered related to the study medication. These preliminary results suggest AD-FX treatment may improve symptoms of ADHD and should encourage further research on the use of ginseng and Ginkgo biloba extracts to treat ADHD symptoms.
    Journal of psychiatry & neuroscience: JPN 06/2001; 26(3):221-8. · 7.49 Impact Factor
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    ABSTRACT: To determine the concentrations of chemical characteristic to extracts of leaves and flowers of Hypericum perforatum (St John's wort) in a number of selected samples and, following chemical characterization, to investigate the effects of these extracts on several pharmacological properties including effects of the extracts on inhibition of 5-hydroxytryptamine (5-HT) uptake and on antioxidant properties. The samples were analyzed for the presence of characteristic chemicals by high performance liquid chromatography (HPLC) directly coupled to ultraviolet wavelength absorbance and positive or negative mode electrospray mass spectrometric detection. The effects of extracts on 5-HT uptake were determined by quantifying 3H-5-HT incorporation into rat hippocampal prisms. Estimates of effects of extracts on free radical scavenging capacity were made using a dynamic assay based on the ability of compounds to prevent the initiation of a colored reaction produced by the horseradish peroxidase catalyzed formation of hydroxyl free radicals from hydrogen peroxide using 2',2'-azinobis (3-ethylbenzthiazoline-6-sulfonic acid) as the color indicator. The chemical profile of a number of extracts were determined and found to differ substantially from each other. Inhibition of 5-HT uptake was found to correlate with hyperforin content and free radical scavenging capacity was found to correlate with the content of several flavonoids including quercetin and hyperoside. Standardized extracts of H perforatum varied substantially in the concentration of several characteristic chemicals. The correlation between pharmacological activity and certain characteristic chemicals found in these extracts indicates that the medicinal benefit derived from selected extracts will vary considerably depending on their chemical composition.
    Acta Pharmacologica Sinica 01/2001; 21(12):1145-52. · 2.50 Impact Factor
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    ABSTRACT: A new competitive enzyme immunoassay for the detection parathyroid hypertensive factor (PHF) in human plasma using a PHF-horseradish peroxidase conjugate and IgM antibody adsorbed on the microtiter plate was established. The antibodies raised against rat PHF could recognize human PHF. Cross-reactivity of anti-PHF antibodies with other serum haptens and proteins was negligible. Conjugation of PHF with horseradish peroxidase did not neutralize the antigen activity. The limit of detection of PHF was 0.02 U/mL in reference units and PHF levels between 0.02 and 1 U/mL could be detected. Within-run coefficient of variation (CV) was less than 10%, and between-run CV was less than 15% for over the dynamic range of the assay. Preliminary clinical studies were performed with plasma samples from hypertensive patients with confirmed diagnosis. Parathyroid hypertensive factor levels, as detected with this immunoassay, were positively correlated with PHF levels detected with the semiquantitative blood pressure (BP) bioassay previously used. Parathyroid hypertensive factor levels detected with the enzyme-linked immunosorbent assay (ELISA) were also correlated with BP in patients. The PHF ELISA provides a selective, simple, and rapid method that can be used for routine determination of PHF in human plasma, and provides useful clinical information.
    American Journal of Hypertension 12/2000; 13(11):1173-9. · 3.40 Impact Factor
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    ABSTRACT: Parathyroid hormone (PTH) and parathyroid hormone-related protein (PTHrP) have been shown to relax various types of smooth muscle, e.g. vascular, uterine and gastric. This study demonstrates that PTH and PTHrP both relaxed cholecystokinin octapeptide (CCK)-induced tension in guinea pig gallbladder strips. This relaxation was concentration-dependent. The use of PTHrP (7-34) blocked the relaxant effect of both agents. This suggested PTH and PTHrP were acting through the same receptor. The use of Rp-cAMPs, an inhibitor of cAMP activation of protein kinase A, and H-89, a selective inhibitor of protein kinase A, suggested that cAMP mediated the relaxant action of PTH and PTHrP. The use of iberiotoxin indicated that the high conductance Ca(2+)-activated potassium channels also mediated the actions of PTH/PTHrP. The use of KT5823, a selective blocker of protein kinase G, also decreased the amount of relaxation induced by PTH/PTHrP. This suggested that crosstalk between the two second messenger (cAMP and cGMP) systems occurred.
    Regulatory Peptides 08/2000; 91(1-3):83-8. · 2.01 Impact Factor
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    ABSTRACT: The effects of Ginkgo biloba leaf extract on rat brain or livermonoamine oxidase (MAO)-A and -B activity, biogenic amine concentration in nervous tissue, N-methyl-D-aspartate (NMDA)- and N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4)-induced neurotoxicity and antioxidant activity was investigated to determine the effects of the extract on monoamine catabolism and neuroprotection. Ginkgo biloba leaf extract was shown to produce in-vitro inhibition of rat brain MAO-A and -B. The Ginkgo biloba extract was chromatographed on a reverse-phase HPLC system and two of the components isolated were shown to be MAO inhibitors (MAOIs). These MAOIs were identified by high-resolution mass spectrometry as kaempferol and isorhamnetin. Pure kaempferol and a number of related flavonoids were examined as MAOIs in-vitro. Kaempferol, apigenin and chrysin proved to be potent MAOIs, but produced more pronounced inhibition of MAO-A than MAO-B. IC50 (50% inhibition concentration) values for the ability of these three flavones to inhibit MAO-A were 7 x 10(-7), 1 x 10(-6) and 2 x 10(-6) M, respectively. Ginkgo biloba leaf extract and kaempferol were found to have no effect ex-vivo on rat or mouse brain MAO or on concentrations of dopamine, noradrenaline, 5-hydroxytryptamine and 5-hydroxyindoleacetic acid. Kaempferol was shown to protect against NMDA-induced neuronal toxicity in-vitro in rat cortical cultures, but did not prevent DSP-4-induced noradrenergic neurotoxicity in an in-vivo model. Both Ginkgo biloba extract and kaempferol were demonstrated to be antioxidants in a lipid-peroxidation assay. This data indicates that the MAO-inhibiting activity of Ginkgo biloba extract is primarily due to the presence of kaempferol. Ginkgo biloba extract has properties indicative of potential neuroprotective ability.
    Journal of Pharmacy and Pharmacology 05/2000; 52(4):451-9. · 2.16 Impact Factor
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    ABSTRACT: Cells dissociated from spontaneously hypertensive rat (SHR) parathyroid glands were grown in culture. Media harvested from the cell cultures were analyzed for parathyroid hypertensive factor (PHF) using the blood pressure bioassay. Cells raised in DMEM containing normal (1.8 mmol/L) CaCl2 secreted a negligible amount of PHF, while cells cultured in Ham's F-12 medium containing low (0.3 mmol/L) CaCl2 secreted higher amounts of PHF. The PHF secretion in Ham's F-12 medium was highest in early passage cells, and was maintained for approximately 12 to 15 passages. PHF purified from the cell culture medium exhibited chromatographic properties identical to those previously described for PHF isolated from SHR plasma or SHR parathyroid gland organ culture medium. These results support the parathyroid gland as the organ of origin of PHF.
    American Journal of Hypertension 01/2000; 12(12 Pt 1-2):1260-3. · 3.40 Impact Factor
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    ABSTRACT: To determine if HT-1001, an extract of American ginseng, affects scopolamine-induced memory and performance deficits in a spatial learning task, alters brain concentrations of aminergic neurotransmitters, and alters choline uptake in synaptosome preparations. Animal study. 48 Sprague Dawley rats. Long-term oral administration of a test material or control solution. Intraperitoneal administration of scopolamine (2 mg/kg) 30 minutes before testing. Performance on Morris water maze task, choline uptake, aminergic neurotransmitter analysis, in vitro monoamine oxidase analysis (of compounds). HT-1001 protected against scopolamine-induced amnesia and increased choline uptake in synaptosomal preparations. HT-1001 did not alter brain concentrations of norepinephrine, dopamine, 5-HT (serotonin), 3,4-dihydroxyphenylacetic acid or 5-hydroxyindoleactic acid. HT-1001 had a very weak ability to inhibit monoamine oxidase activity in vitro. HT-1001 demonstrates a capacity to protect against scopolamine-induced memory deficits.
    Journal of psychiatry & neuroscience: JPN 12/1999; 24(5):442-52. · 7.49 Impact Factor
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    ABSTRACT: We have previously elucidated the opiate-like action of mitragynine, an active principle isolated from the Thai medicinal plant Mitragyna speciosa. In the present study, effects of the related compound, mitragynine pseudoindoxyl on electrically stimulated contraction in guinea pig ileum and mouse vas deferens, and on its binding affinity in the guinea pig brain membranes were studied. Mitragynine pseudoindoxyl inhibited the electrically stimulated ileum and mouse vas deferens contractions in a concentration-dependent manner. In the ileum, the effective concentration is in an nM order, being nearly equivalent to reported concentrations of the micro-opioid receptor agonist [D-Ala2, Met-Phe4, Gly-ol5] enkephalin (DAMGO), and is 100- and 20-fold smaller than those of mitragynine and morphine, respectively. In the vas deferens, it is 35-fold smaller than that of morphine. The inhibitory action of mitragynine pseudoindoxyl in the ileum was antagonized by the non-selective opioid receptor antagonist naloxone and the micro-receptor antagonist naloxonazine. It was also antagonized by the delta-receptor antagonist naltrindole in the vas deferens. Mitragynine pseudoindoxyl showed a similar binding affinity to DAMGO and naltrindole at micro- and delta-receptors, respectively. However, the affinity at kappa-receptors was negligible. The present study demonstrates that mitragynine pseudoindoxyl, a novel alkaloid structurally different from other opioid agonists, acts on opioid receptors, leading to a potent inhibition of electrically stimulated contraction in the ileum through the micro-receptors and in mouse vas deferens through delta-receptors.
    General Pharmacology 08/1999; 33(1):73-81.
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    ABSTRACT: Rutaecarpine (Rut) has been shown to induce hypotension and vasorelaxation. In vitro studies indicated that the vasorelaxant effect of Rut was largely endothelium-dependent. We previously reported that Rut increased intracellular Ca2+ concentrations ([Ca2+]i) in cultured rat endothelial cells (ECs) and decreased [Ca2+]i in cultured rat vascular smooth muscle (VSMCs) cells. The present results showed that the hypotensive effect of Rut (10-100 microgram/kg i.v.) was significantly blocked by the nitric oxide synthase inhibitor Nomega-nitro-L-arginine. In aortic rings, Rut (0. 1-3.0 microM)-induced vasorelaxation was inhibited by Nomega-nitro-L-arginine and hydroquinone but not by antagonists of the various K+ channels, 4-aminopyridine, apamin, charybdotoxin, or glibenclamide. Rut (0.1 and 1.0 microM) inhibited the norepinephrine-induced contraction generated by Ca2+ influx and at 1.0 microM increased cyclic GMP (cGMP) production in endothelium-intact rings and to a lesser extent in endothelium-denuded rings. In whole-cell patch-clamp recording, nonvoltage-dependent Ca2+ channels were recorded in ECs and Rut (0.1, 1.0 microM) elicited an opening of such channels. However, in VSMCs, Rut (10.0 microM) inhibited significantly the L-type voltage-dependent Ca2+ channels. In ECs cells, Rut (1.0, 10.0 microM) increased nitric oxide release in a Ca2+-dependent manner. Taken together, the results suggested that Rut lowered blood pressure by mainly activating the endothelial Ca2+-nitric oxide-cGMP pathway to reduce smooth muscle tone. Although the contribution seemed to be minor in nature, inhibition of contractile response in VSMCs, as evidenced by inhibition of Ca2+ currents, was also involved. Potassium channels, on the other hand, had no apparent roles.
    Journal of Pharmacology and Experimental Therapeutics 07/1999; 289(3):1237-44. · 3.86 Impact Factor
  • P.K.T Pang, L W Kline
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    ABSTRACT: Pituitary adenylate cyclase activating polypeptide (PACAP) was shown to relax guinea pig gallbladder strips contracted with cholecystokinin. This relaxation was mediated by PACAP interacting with VIP/PACAP receptors. PACAP was also shown to cause contraction in guinea pig gallbladder strips. The present study demonstrated that calphostin C and bisindolylmaleimide IV, both blockers of protein kinase C, significantly reduced tension, Rp-adenosine 3', 5'-cyclic monophosphatase triethylamine, a blocker of protein kinase A, had no effect on PACAP-induced tension. Nifedipine also significantly reduced the PACAP effect. The contractile effects of PACAP are mediated by protein kinase C.
    Regulatory Peptides 11/1998; 77(1-3):63-7. · 2.01 Impact Factor
  • J Ji, C G Benishin, P K Pang
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    ABSTRACT: The present study was designed to investigate whether nitric oxide (NO) could interfere with intracellular Ca++ release through different pathways in vascular smooth muscle. Phasic contractions of rat aorta induced by phenylephrine or caffeine in Ca++-free solution were used as an indicator of intracellular Ca++ release through the inositol 1,4,5-triphosphate receptor pathway and the ryanodine receptor pathway, respectively. In addition, cytoplasmic Ca++ concentration ([Ca++]i) in vascular smooth muscle cells was determined by fluorescence measurement. Acetylcholine (ACh) inhibited the phenylephrine-evoked phasic contractions in Ca++-free solution in endothelium-intact but not -denuded aortic rings in a dose-dependent manner. However, ACh did not affect the action of caffeine. The inhibition by ACh was blocked completely by the NO synthase inhibitor Nomega-nitro-L-arginine, which could be reversed totally by L-arginine but not D-arginine. Methylene blue, a soluble guanylate cyclase inhibitor, also abolished the inhibition by ACh. Sodium nitroprusside, an NO donor, attenuated the phenylephrine- but not caffeine-induced phasic contractions in denuded aortic rings in Ca++-free solution. The effect of sodium nitroprusside was reversed substantially by methylene blue. Furthermore, sodium nitroprusside inhibited the elevation of [Ca++]i induced by phenylephrine in vascular smooth muscle cells isolated from rat aorta in the absence of extracellular Ca++, which could be abolished significantly by methylene blue. These results suggest that NO selectively inhibits intracellular Ca++ release stimulated by inositol 1,4,5-triphosphate, but not caffeine in vascular smooth muscle.
    Journal of Pharmacology and Experimental Therapeutics 04/1998; 285(1):16-21. · 3.86 Impact Factor
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    L W Kline, M L Zhang, P K Pang
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    ABSTRACT: Cholecystokinin octapeptide (CCK), acetylcholine (ACh) and ceruletide have been shown to produce contraction in bullfrog (Rana catesbeiana) gallbladder strips. Agents capable of relaxing the bullfrog gallbladder are less numerous. Calcitonin gene-related peptide reduced the amount of both CCK- and ACh-induced tension in bullfrog gallbladder strips. The purpose of this study was to determine whether vasoactive intestinal peptide (VIP), nitric oxide (NO) and the second messengers cyclic GMP or cyclic AMP had any effect on gallbladder motility in the bullfrog. In vitro tension studies using l-NG-nitro-arginine methyl ester, Methylene Blue, sodium nitroprusside and N2,2'-O-dibutyryl guanosine 3',5'-cyclic monophosphate suggested that nitric oxide did not modulate gallbladder motility in the bullfrog gallbladder. Histochemical staining for NADPH diaphorase (nitric oxide synthase) failed to demonstrate nerve fibers containing nitric oxide synthase in the bullfrog gallbladder. In vitro studies demonstrated that VIP had no effect on CCK-induced tension. However, in vitro studies using either 8-bromoadenosine 3',5'-cyclic monophosphate or forskolin demonstrated that both agents relaxed strips precontracted with CCK. The results of this study suggested that, while neither NO nor VIP had a role in modulating bullfrog gallbladder motility, cyclic AMP was capable of modulating bullfrog gallbladder motility.
    Journal of Experimental Biology 11/1997; 200(Pt 20):2669-74. · 3.00 Impact Factor
  • Loren W Kline, Peter K.T Pang
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    ABSTRACT: Calcitonin gene-related peptide (CGRP) has been shown to relax cholecystokinin-induced tension in guinea pig gallbladder strips. This relaxation is dependent on the concentration of CGRP, and is primarily due to the opening of ATP sensitive K+ channels; however, other mechanisms may also be involved. Studies using forskolin, 8-bromoadenosine 3', 5' cyclic monophosphate, dibutyryl cAMP, cholera toxin, and Rp-adenosine 3', 5'-cyclic monophosphothioate triethylamine, which measured changes in tension suggest that cAMP may be involved in mediating the actions of CGRP. Radioimmunoassay of strips precontracted with cholecystokinin octapeptide (CCK) and either treated with CGRP or its solvent demonstrated that cAMP concentrations increased with CGRP treatment. The results of these studies demonstrate that CGRP acts through multiple mechanisms to induce relaxation of guinea pig gallbladder strips precontracted with CCK.
    Regulatory Peptides 10/1997; 72(1):55-9. · 2.01 Impact Factor
  • J J Shan, B Li, N Taniguchi, P K Pang
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    ABSTRACT: Pharmacological doses of 24R,25-dihydroxyvitamin D3 (24,25D3) inhibited both phasic and tonic contraction of Sprague-Dawley (SD) rat tail artery helical strips induced by KCl, norepinephrine (NE), and arginine vasopressin (AVP) in organ-bath studies. 24,25D3 also decreased the tension dependent on external calcium influx induced by KCl, AVP, and NE and the tension dependent on internal calcium release from intracellular calcium stores induced by NE. In vascular smooth muscle cells isolated from SD rat tail artery, 24,25D3 reduced membrane L-type calcium channel current and the increment of intracellular calcium concentration induced by KCl. It is suggested that 24,25D3 directly relaxed precontracted SD rat-tail artery by its inhibitory effect on plasma membrane and intracellular organelle calcium channels.
    Steroids 12/1996; 61(11):657-63. · 2.72 Impact Factor
  • P K Pang, J J Shan, K W Chiu
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    ABSTRACT: Tetramethylpyrazine (TMP) is a compound purified from a medicinal plant Ligusticum wallichii Franch. Its effects on in vivo blood pressure, in vitro vascular contractility, and intracellular calcium regulation in rats were examined in the present study to see if it was a possible calcium antagonist in the vascular tissue. Data showed that TMP was hypotensive and had a direct vascular effect. It not only blocked the entry of extracellular calcium through calcium channels but also inhibited the release of intracellular stored calcium in the vascular smooth muscle cell. It was a true calcium antagonist.
    Planta Medica 11/1996; 62(5):431-5. · 2.34 Impact Factor
  • Journal of Hypertension 10/1996; 14(9):1053-60. · 4.22 Impact Factor
  • J Xiao, P K Pang
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    ABSTRACT: We previously showed that the lymphocyte proliferation response was significantly suppressed in spontaneously hypertensive rats (SHR) and that this depressed response was due to excessive production of nitric oxide (NO) in macrophages and vascular smooth muscle cells (VSMC). Whether lymphocyte depression and activation of NO synthesis are related to age and development of hypertension remains unclear. The present study addresses such a correlation by examining the time course of development of hypertension, NO synthesis alteration and lymphocyte depression in SHR. Our results show that 1) SHR spleen cell proliferation responses are depressed at 4, 8, and 12 weeks and 1 year of age, with the lowest response occurring at 4 weeks of age; 2) this depressed response is corrected by either NO synthase inhibitor or removal of macrophages from spleen cells; 3) NO production by SHR spleen macrophages is significantly higher in all age groups; 4) upon stimulation with lipopolysaccharide or cytokines, SHR VSMC produce a significantly greater amount of NO in all age groups; 5) the increase in NO synthesis in VSMC correlates significantly with the rise in blood pressure in SHR. However, statistical correlation analysis suggests that lymphocyte depression and the alteration of NO synthesis in macrophages were not associated with either age or increased blood pressure in SHR. On the contrary, the activation of NO synthesis in VSMC can be statistically correlated with elevated blood pressure throughout the development of hypertension in SHR. Nevertheless, the results also suggest that a general alteration in the NO synthesis system may exist in SHR.
    American Journal of Hypertension 05/1996; 9(4 Pt 1):377-84. · 3.40 Impact Factor

Publication Stats

2k Citations
476.81 Total Impact Points


  • 1986–2002
    • University of Alberta
      • • Department of Physiology
      • • Division of Endocrinology
      Edmonton, Alberta, Canada
    • Jinan University (Guangzhou, China)
      Shengcheng, Guangdong, China
  • 1999
    • National Research Institute of Chinese Medicine
      T’ai-pei, Taipei, Taiwan
  • 1995
    • Università degli studi di Palermo
      • Department of internal medicine and medical specialties (DIMIS)
      Palermo, Sicily, Italy
  • 1994
    • Wayne State University
      • Department of Internal Medicine
      Detroit, MI, United States
  • 1993
    • Cornell University
      • Cardiovascular Center
      Ithaca, NY, United States
  • 1983–1992
    • The Chinese University of Hong Kong
      • Department of Biology
      Hong Kong, Hong Kong
  • 1989–1991
    • Radboud University Nijmegen
      • Department of Organismal Animal Physiology
      Nijmegen, Provincie Gelderland, Netherlands
    • Johns Hopkins Medicine
      • Department of Environmental Health Sciences
      Baltimore, MD, United States
  • 1980–1989
    • Texas Tech University Health Sciences Center
      El Paso, Texas, United States
  • 1988
    • Hospices Civils de Lyon
      Lyons, Rhône-Alpes, France
  • 1984
    • Columbia University
      New York City, New York, United States
    • University Medical Center Health System
      Lubbock, Texas, United States